The first cross-species mechanism of microbial metabolism driving distal tumors is revealed (Nature. 2024 Aug;632(8027):1137-1144.)
Article Gut microbiota carcinogen metabolism causes distal tissue tumours
The newly published article "Gut microbiota carcinogen metabolism causes distal tissue tumours" in Nature reveals the key role of gut microbiota in environmental carcinogen-induced tumors.
Through mouse models, sterile animal experiments and in vitro culture of human gut microbiota, it is confirmed that gut microbes can metabolize nitrosamine carcinogens (such as BBN) to produce genotoxic metabolites (such as BCPN), thereby promoting the occurrence and progression of distal tissue (such as bladder) tumors.
The study found that there are individual differences in microbial metabolic capacity and identified the key role of specific strains (such as Escherichia coli), which provides a new idea for cancer risk assessment and prevention strategies based on gut microbiota.
Welcome to discuss the universal mechanism of microbial-carcinogen interaction in tumorigenesis and the prospects for clinical transformation.
Technical highlights of this article.
Multi-dimensional model construction
Combined with antibiotic-treated mouse model, germ-free (GF) mouse colonization experiment and humanized mouse model, the effect of intestinal microorganisms on carcinogen metabolism was systematically verified.
Using metabolic cage experiment and LC-MS quantitative analysis, the dynamic distribution of carcinogens (BBN) and their metabolites (BCPN) in tissues and excreta was tracked.
Microbial function analysis technology
Intestinal strains with BBN metabolism ability (such as Escherichia coli and Staphylococcus) were identified through 16S rRNA sequencing and whole genome sequencing.
Using in vitro anaerobic/microaerobic culture system, the microbial oxidation and deglucuronidation of BBN were verified by simulating the intestinal environment.
Cross-species comparison method
Comparative analysis of the differences in BBN metabolism between mouse and human intestinal flora revealed the species conservation and individual heterogeneity of metabolic ability.
Article Gut microbiota carcinogen metabolism causes distal tissue tumours
I have a question:
Although antibiotic treatment reduces tumor incidence, it may also affect the activity of the host's own metabolic enzymes (such as CYP450). Can the interference of host metabolism be ruled out?
Any ideas can tell this?
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